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The AAA+ protein torsinA interacts with a conserved domain present in LAP1 and a novel ER protein
A glutamic acid deletion (ΔE) in the AAA+ protein torsinA causes DYT1 dystonia. Although the majority of torsinA resides within the endoplasmic reticulum (ER), torsinA binds a substrate in the lumen of the nuclear envelope (NE), and the ΔE mutation enhances this interaction. Using a novel cell-based...
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| Main Authors: | , |
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| Format: | Artigo |
| Sprog: | Inglês |
| Udgivet: |
The Rockefeller University Press
2005
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| Fag: | |
| Online adgang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2171781/ https://ncbi.nlm.nih.gov/pubmed/15767459 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1083/jcb.200411026 |
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